Abstract

Objective: There are limited data regarding the characteristics of intracranial plaques according to stroke mechanism in the posterior circulation. This study aims to compare whether the plaque characteristics and baseline features are different in patients with artery-to-artery (A-to-A) embolism and those with parent artery disease in the intracranial vertebrobasilar atherosclerotic disease.Methods: From September 2014 to January 2017, patients with recent posterior circulation stroke due to intracranial vertebrobasilar atherosclerotic disease were retrospectively analyzed. Patients with the following eligibility criteria were included: (1) age ≥18 years old, (2) ischemic stroke in the vertebrobasilar territory, (3) 70–99% stenosis of the intracranial vertebral artery or basilar artery, and (4) two or more atherosclerotic risk factors. Patients with concomitant ipsilateral or bilateral extracranial vertebral artery >50% stenosis, cardio-embolism, or non-atherosclerotic stenosis were excluded. The plaque characteristics, including intraplaque compositions (intraplaque hemorrhage and intraplaque calcification), intraplaque enhancement, and remodeling index, were evaluated by using 3T high-resolution magnetic resonance imaging (HRMRI). The baseline features including vascular risk factors and the involved artery were collected. Patients were divided into A-to-A embolism and parent artery disease groups based on the diffusion-weighted images, T2-weighted images, or computed tomography. The plaque characteristics and baseline features were compared between the two groups.Results: Among consecutive 298 patients, 51 patients were included. Twenty-nine patients had A-to-A embolism and 22 patients had parent artery disease. Compared with parent artery disease, the occurrence rates of intraplaque enhancement and intracranial vertebral involvement were higher in the A-to-A embolism group (79.3 vs. 36.4%; p = 0.002 and 62.1 vs. 18.2%; p = 0.002, respectively). Multivariable logistic regression analysis showed that intraplaque enhancement and intracranial vertebral artery plaques were also associated with A-to-A embolism (adjusted OR, 7.31; 95% CI 1.58–33.77; p = 0.011 and adjusted OR, 9.42; 95% CI 1.91–46.50; p = 0.006, respectively).Conclusion: Intraplaque enhancement and intracranial vertebral artery plaques seem to be more closely associated with A-to-A embolism than parent artery disease in patients with symptomatic intracranial vertebrobasilar disease.Clinical Trial Registration:http://www.clinicaltrials.gov, identifier: NCT02705599.

Highlights

  • Posterior circulation stroke accounts for about 20–25% of ischemic stroke [1, 2], 9.9–16.3% of which is due to intracranial vertebrobasilar stenosis [3, 4]

  • Detailed infarct distributions and magnetic resonance angiography (MRA)/computed tomography angiography (CTA)/digital subtraction angiography (DSA) of included patients are presented in Supplementary Figure 1

  • In patients with symptomatic severe intracranial vertebrobasilar atherosclerosis, we found that the patients with A-to-A embolism were more likely to have a higher occurrence of intraplaque enhancement and a higher rate of intracranial vertebral artery involvement than those with parent artery disease

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Summary

Introduction

Posterior circulation stroke accounts for about 20–25% of ischemic stroke [1, 2], 9.9–16.3% of which is due to intracranial vertebrobasilar stenosis [3, 4]. Patients with the symptomatic vertebrobasilar disease with evidence of impaired distal perfusion or blood flow due to severe stenosis are at a higher risk of recurrence with medical treatment [4,5,6]. In these patients, the stroke mechanisms are usually impaired distal perfusion combined with A-to-A embolization or parent artery disease [7]. Studies on that whether the crucial plaque characteristics are different in patients with A-to-A embolism and those with parent artery disease due to severe intracranial vertebrobasilar stenosis are scarce. A few studies are unraveling the differences of the plaque features by using HRMRI between different stroke mechanisms in patients with anterior circulation stroke [18, 19], but is rarely studied in the posterior circulation

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